Good news but feeling so sad

Hi everyone, first time posting on this forum. Thanks for listening.

I went to the endo yesterday, and got the good news that my A1C dropped from 10.6 to 8.2. I was feeling pretty good about it. This morning I was texting my dad and he said “That’s great, we need to celebrate!” and I just felt this overwhelming sadness and started to cry.

I’ve been type 1 for 14 years now, and had my fair share of ups and downs. I don’t know why I’m feeling this way, seemingly because of good news. If anyone has any thought I would love to hear them!

Thank you,


I suggest it is not sadness it is a mixture of relief and a recognition of how much more you have to do. Celebration is appropriate, so are tears. For me the only reaction I cannot do with good diabetes news, is to stop trying.


I don’t have any wise advice, but I want to congratulate you on your efforts to bring your A1c down. It is never easy to make a lifestyle change so give yourself a pat on the back.


Yes, celebrate, you have done so well and I am sure yo will keep up the good work. Congratulations.


I have always been suspicious of A1c results, since they pretend to measure something they cannot, which is the exact correlation between hyperglycemia and diabetic complications. Since it has been established that genetics, continuing autoimmunity, and hypoglycemia all contribute to producing the distinct vascular and neurological changes of diabetes, as well as helping to determine how much impact any given degree of hyperglycemia will have, the A1c number in itself doesn’t say much.

We also don’t know how much of the damage of hyperglycemia is caused by any given range of excess glucose in the blood, so it may well be that 90% of the damage is done just by having an A1c value between 5 and 7, which would make adequate control impossible. Supporting the theory that even low levels of hyperglycemia may be decisive in causing complications is the fact that evolutionary processes induce the human body not to expend any energy to do things which are not necessary, barring a few oddities of the body which are vestiges of the evolutionary process, such as our vestigial tail, the coccyx, which is no help any more but which the body still expends energy to make. So if the body makes such a vigorous and elaborate effort to keep blood sugar so very close to an A1c of 5 all the time, doing this must be vitally important, and not being able to do it must be very significant. I know that in my own case, when I was first diagnosed as a type 1 diabetic in 1966, after an extremely rapid onset of the symptoms, I was tested in an experiment and found already to have developed a significant slowing of nerve conduction velocities, indicating that even just a week of hyperglycemia, producing a even just a tiny burden of excess glucose, can cause diabetic nerve damage.

WOW! What a killjoy! Knowing how hard type 1 diabetes management can be, everyone on this forum needs to be encouraged for their triumphs no matter how small; not made to feel defeated.


While a drop of over 2 points on the A1c is certainly cause for celebration, even an 8.2 is high enough that it could be affecting both your physical energy and your mood.

And while A1c is an important number, it tells you nothing about the swings from high to low. So, consider how your sugar levels affect your mood.

We all put value judgements on whether things are good or bad. Given similar situations, we may well come to different conclusions. “I’m down over two points - yes!” Or “two points is nice, but I tried so hard and progress is so slow.” Or perhaps the sadness is really only marginally related to a number. How was your mood prior to obtaining the news? How did you interpret what your Dad said? Did YOU feel it was cause for celebration? Why or why not?

In any event, your improvement in A1c is significant. Even if you feel sad, your continued efforts to achieve better control will pay off. Congratulations on having made a significant improvement.


yeah no kidding lol… Thank you for your kind words Cinderfella!


That is unforntunate that you had nerve damage so quickly. However, I wasn’t asking about the validity or importance of A1C results, those questions I would certainly ask my doctor and not on a forum. I was asking more about the emotional response that I had to the seemingly good news, and if anyone had any insight into that.

I’m trying to do better with my diabetes, and posts like this don’t help. I don’t know if you’re trying to shame me for my A1c or what, but it is still an important measure that doctors use to assess their patients. Seeing as most people don’t have nerve damage after “1 week” of diabetes, I think in your case it could be related to other things. I’ve had diabetes for 14 years and don’t have any nerve damage- and that is with my A1C currently at 8.2.

As to your other points, I understand the concept of homeostasis. I don’t understand what the vestigial tail and coccyx added to your argument. Obviously diabetes is a disease and in this case that means disrupting the body’s normal homeostatic functions. That is why we have to manage the disease? I’m not perfect and I know I have a long way to go. In the future please consider if you’re adding something helpful to the forum.


I have a hard time picturing diabetes and celebrating in the same sentence. While every little victory should be celebrated, sometimes it’s difficult to celebrate when, despite your success, you still have to do more of the same tomorrow. It’s always more fun to celebrate when the hardship is over, right?

All the same, congrats on lowering your A1c! That’s a big jump!

P.S. There are lots of productive, helpful discussions on the forum about the A1c vs. time in range. It’s also been interesting to see the discussions about how some people naturally tend toward higher A1c’s despite their blood sugars indicating that their A1c should be lower. Obviously your doctor’s input should be valued, but don’t write all of us off :slight_smile:


Bronte, I quite obviously wasn’t attacking anyone in my comment, but just discussing the scientific significance of A1c values generally. My point about the vestigial tail bone in modern humans was just that this is a rare exception to the usual rule that nature does nothing in vain, which I was discussing for its implications for the fact that nature expends so much energy keeping blood sugars in the 5 range, which it would not do unless keeping levels close to 5 were very important.

When I was first diagnosed I was asked to participate in a study being conducted by Dr. Donna Younger on nerve conduction velocities in newly diagnosed type 1 diabetics. Electrodes were placed all over the body and recordings were made of any deviations from the normal values. All participants were given the results after they were published, and all of us had been found to have experienced a delaying of nerve conduction velocities even after the miniscule burden of hyperglycemia experienced by diagnosis.

Seydlitz, Do you have any evidence that your BGs were normal before your rapid onset of symptoms? You could have had elevated BGs for months, even years, but just not high enough to cause symptoms.


It is the onset of winter and the early darkness has me kinda dazed and sad too. Especially when I leave for work in the dark and don’t get back home till its dark. “Seasonal depression” is what they call it. Sometimes I blame it on something (like diabetes) but really I think that’s unfair of me to blame something like that.

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That’s simply not supported by the DCCT and other results. An A1C of 9 is clearly a much bigger risk than an A1C of 7. At same time an A1C of 11 is an exponentially larger risk than 9. Any improvement in A1C is a good thing.



Because of an extensive family history of type 1 diabetes, I had been taken to the hospital to be tested for type 1 diabetes in September, 1966, and had been found not to have it. But then just a few days before Hallowe’en at the end of October, about a month after the test (I remember it was the day of the very first showing of the Charlie Brown Hallowe’en special), I noticed I was urinating and drinking too much. Given the family history, I was aware of the symptoms of diabetes, and my father, who never developed diabetes, always kept some urine sugar test strips in the bathroom. So I tested my urine and found that I had a value of +1, which indicated a moderate level of sugar in the urine. I told my mother about it, and by Friday I was diagnosed as a diabetic, so the time between the initial symptoms and the diagnosis was minimal.

I should also add that type 1 diabetes is characterized by its rapidity of onset, and all the other newly-diagnosed patients in Dr. Younger’s study were found to have a distinct slowing of nerve conduction velocities.

It quite obviously is not quite obvious that you weren’t attacking anyone based upon @Bronte’s reply. I myself wonder how a discussion of the validity of an A1C was spurred based upon the OP and encourage you to start new discussions when your thoughts are not directly responsive to the topic at hand - the discussion is valid, just not appropriate right here, IMO.

@Bronte - Diabetes is hard, and it’s emotional. You’ve had a phenomenal improvement in A1C. Even if it isn’t a precise measurement of success, the direction and magnitude of the change can not be argued with. It’s a daily, unrelenting struggle, and your reaction could be as others suggest, just a release of anxiety, stress, relief, joy or knowing that although it’s one step closer, you still need to keep going.

I love your dad’s response! I agree! Celebrate and keep going! Every step forward deserves accolades!!


In 1966 the cutoff for a Dx of diabetes was a fasting level over 140. I know type 1 usually comes on quickly, but I wonder how many people were having fastings in 130s and high postprandial levels, enough to cause neuropathy without a Dx.



A more common interpretation of the standards of the 60’s, was that sugar in urine was the definition of diabetes. T1 onset in kids can be so fast that it’s hard to catch in the early stages.

Also keep in mind that the standard of care was so poor up through the 1990’s, that the WESDR group reported “retinopathy will be present in nearly all persons with type 1 diabetes by 10 years duration and in all persons with diabetes by 20 years duration”.

Up until the DCCT there was no collected data that showed average bg’s (or A1C’s) were at all related to complications, and a lot of my doctors before then thought that impurities in insulin was the cause of all the complications.

Stone knives and bearskins, man!


In September of 1966 I was given an oral glucose tolerance test to determine my susceptibility to ‘juvenile diabetes,’ as it was called at the time, and the test result was negative. But then, just a month later, I was diagnosed with the disease, so at least in my case, there must have been very little accumulation of hyperglycemic damage before I was found to have delayed nerve conduction velocities, suggesting either that miniscule excesses of glucose can already produce measurable damage, or that other factors are involved in causing the complications of type 1 diabetes, such as the continuation of the same autoimmunity that causes the beta cell destruction, or genetic influences inherited along with the cluster of genes that determine susceptibility to type 1 diabetes.

B. Fierro, et al., “Nerve Conduction Velocity and Circulatory Immunocomplexes in Type 1 Diabetic Children,” Acta Neurologica Scandinavica, 83 (3) 176-178 (1991) and N. Janahi, et al., “Diabetic Peripheral Neuropathy. Is It an Autoimmune Disease?” Immunology Letters, 106 (1) 73-76, among others, suggest that diabetic nerve disease may be caused by the same autoimmune processes which cause the beta cell destruction, which would explain the results in Donna Younger’s experiment which found slowing of nerve conduction velocities in newly-diagnosed patients despite the minimal impact of hyperglycemia when these patients presented.

S. Yigit, et al., “Association of MTHFR Gene C6777 Mutation with Diabetic Peripheral Neuropathy and Diabetic Retinopathy,” Molecular Vision, 19, 1626-1630 (2013) and J. Hoeijmakers, et al., “Channelopathies, Painful Neuropathy, and Diabetes: Which Way Does the Causal Arrow Point?” Trends in Molecular Medicine, 20 (10) 544-550 (2014), among others, suggest that genes inherited along with those inducing the susceptibility to type 1 diabetes may also cause diabetic neuropathy, which would also explain why the group of patients I was with in 1966 was found to have measurably slowed nerve conduction velocity even though we had had very little exposure to hyperglycemia.

In staging studies of the development of type 1 diabetes, in the first prodromal stage the appearance of autoimmune antibodies has been found a good 5 years prior to the diagnosis of the disease. However, only in the second stage has an abnormal response to a glucose tolerance test been found, meaning that while these patients do not yet have frank hyperglycemia, they do show it after an intense glucose challenge, meaning that they might be showing hyperglycemia after binging on sweets in this period. In fact, their HbA1c values can be very slightly elevated in this period, from 10% to 20% higher than normal, which is still a very low level. The duration of their exposure in the second stage before the disease appears is quite short, since it has been found that the “2-h [hour] OGTT [oral glucose tolerance test] glucose levels … did not begin to change until approximately 0.8 years before diagnosis … .” (Richard Insel, et al., “Staging Presymptomatic Type 1 Diabetes,” Diabetes Care, 38 (10) 1964-1974 (2013)).

What this all means is that insofar as there is any burden of hyperglycemia on the patient before diagnosis of type 1 diabetes, it is very small and very brief, so that if even this small amount of hyperglycemia can cause measurable damage, patients with established cases of type 1 diabetes would have to achieve an impossibly meticulous degree of control to avoid complications.

>Also keep in mind that the standard of care was so poor up through the 1990’s, that the WESDR group reported “retinopathy will be present in nearly all persons with type 1 diabetes by 10 years duration and in all persons with diabetes by 20 years duration”.

Yes. A friend’s son was told he’d be blind by the age of 30.

I have another friend whose father got type 1 before they discovered insulin. He was on the Allen Starvation Diet, and as a result, at the age of 12, he weighed 45 pounds. But he was convinced they’d find a cure and he wanted to be alive when they did. He was, got insulin, and lived to grow up and have children. But his letters, which my friend has, are sad. One day he was ecstatic because they were going to allow him a second cube of cheese. I think of that if I’m feeling sorry for myself because I can’t eat ice cream.

A friend was in the DCCT. He took my BG the first day post-Dx, when my fasting was about 300. The sugar in my urine was so high they thought their machine was broken. But I felt fine. I think A1c was about 13 (they only measured A1, which was 16, I think.)

>Up until the DCCT there was no collected data that showed average bg’s (or A1C’s) were at all related to complications

It’s stunning how uninformed they were. I wonder what else they’ll discover that will make them be surprised at what we’re doing just us as we’re surprised at old treatment methods.